Anesthesia is the loss of sensation in the body induced by the administration of a drug. There are many risks associated with the drug-induced loss of sensation and without proper equipment and skilled operators, complications often occur. Because there are risks associated with anesthesia, it is preferable that an anesthetized patient emerge from anesthesia and that ventilatory drive be restored as soon as possible.
The ability of patients to breathe on their own upon emergence from anesthesia is dependent upon three conditions. First, the blood concentration of anesthetic agent must be low, less than about 0.2% for isoflurane. This is achieved by turning off the anesthetic agent, washing the agent from the breathing circuit, and ventilating the patient with a normal minute volume for several minutes. "Minute volume" is the total volume of gas delivered to or expired by a patient over one minute. Hyperventilation can be used to accelerate the process of removing the anesthetic agent from the body. However, hyperventilation causes CO.sub.2 to be expired from the lung and lowers the partial pressure of CO.sub.2 (PCO.sub.2) in the blood, P.sub.a CO.sub.2 (arterial blood carbon dioxide tension).
Second, if a neuromuscular function blocking drug had been used, it must be adequately reversed for sufficient ventilatory muscle strength to return. This is accomplished pharmacologically.
Third, the P.sub.a CO.sub.2 must be high enough to adequately stimulate the central ventilatory center in the brain. The ventilatory response to CO.sub.2 is a continuous function, but, a P.sub.a CO.sub.2 between 35 mmHg and 44 mmHg is normally required to stimulate ventilatory efforts in the patient recovering from anesthesia.
Unfortunately, increasing P.sub.a CO.sub.2 by hypoventilation can lead to complications such as hypoxia. Also, the awakening process is actually prolonged by the failure to remove anesthetic agent from the patient's body. Thus, the clinician is faced with a dilemma; the clinician must both remove the anesthetic agent by hyperventilation and increase the arterial blood carbon dioxide tension, P.sub.a CO.sub.2, by hypoventilation.
Some anesthesia machines have been manufactured with a valve that allows bypassing the CO.sub.2 absorber in a circle system breathing circuit. Bypassing the CO.sub.2 absorber permits the patient to rebreath expired CO.sub.2 gases thus the PCO.sub.2 rises in the inspired gas. However, this does not substantially hasten awakening because if the system is mostly closed, anesthetic agent is also recirculated to the patient. Therefore, even though the patient is able to rebreath expired CO.sub.2 and thereby increase the arterial blood carbon dioxide tension, the patient also rebreaths expired anesthesia agent. If the system was mostly open, little rise in PCO.sub.2 can be achieved. Also, such a design requires the clinician to remember to shut off the bypass, before the next procedure. Failure to turn off the bypass, however, was not an infrequent occurrence and occasionally contributed to complications.
In order to increase the P.sub.a CO.sub.2 of a patient, it is helpful to measure P.sub.a CO.sub.2. While measurements of CO.sub.2 from the expired breathing gas have long been used to estimate the P.sub.a CO.sub.2, this information has not been used to rapidly restore ventilatory drive to a patient after anesthesia. The gas at the end of each tidal ventilation is assumed to be in equilibrium with the arterial blood. Hence, the end-tidal CO.sub.2 partial pressure, P.sub.ET CO.sub.2, is often used to estimate P.sub.a CO.sub.2. For example, U.S. Pat. No. 4,423,739 to Passaro et al. discloses an apparatus for determining the partial pressure of CO.sub.2 in the arterial blood of a patient by measuring carbon dioxide concentration at the end-tidal of a patient's exhaled breath.
The practice of using the partial pressure of CO.sub.2 in the arterial blood of a patient to control respiration has been in use for several years. For example, U.S. Pat. No. 4,112,938 to Jeretin discloses a device for controlling patient respiration in accordance with the partial pressure of CO.sub.2 in the arterial blood or tissue measured in the alveolar expiration air. The Jeretin patent states that low arterial CO.sub.2 content resulting from hyperventilation is brought to a standard value by increasing CO.sub.2 content in the inspiration air. The CO.sub.2 in this system comes, however, from the patient's own expired gas, not from an external source. Control of this process is based on a continuous measuring of the partial pressure of CO.sub.2. The serious problems associated with anesthesiology and in particular restoring the ventilatory drive of a patient are not addressed by the Jeretin patent.
Previous attempts to restore the ventilatory drive to an anesthetized patient involves such things as bypassing the CO.sub.2 absorber. This technique, while partially effective in raising the CO.sub.2 in the inspired mixture has the problem of reintroducing the anesthesia agent to the patient. For example, in the Jeretin device, the patient rebreathes anesthetic agent as well as the CO.sub.2. Such a process inhibits resuscitation of the patient. It is one object of the present invention to solve this problem. Furthermore, as rebreathing limits the inspired PCO.sub.2 to the patient's mean expired PCO.sub.2, the CO.sub.2 concentration may not be high enough to raise the P.sub.a CO.sub.2 to the desired level rapidly and reliably. It is the object of the present invention to also solve this problem. Yet another object of the invention is to provide a system which is automated to enable effective emergence from anesthesia while minimizing the risk of operator error. It is yet a further object of the invention to optimize the introduction of CO.sub.2 to a patient to minimize risks and complications associated with prolonged anesthesia.